Regulated transcription of c-Ki-ras and c-myc during compensatory growth of rat liver.

Goyette, M; Petropoulos, Christos J.; Shank, Peter R.; Fausto, Nelson

doi:10.1128/mcb.4.8.1493

Cited by 205 publications

(99 citation statements)

References 40 publications

(27 reference statements)

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“…31 The protooncogene increases in the regenerating rat liver and its inhibition interferes with cell cycle progression after PH in rats. 13,32,33 In our experiments, ras increased similarly in the livers of both CYC202-and DMSO-treated rats after PH. Ras might also provide a link between the cyclin D/Cdk4 and the cyclin E/Cdk2 complex in cycling hepatocytes.…”

Section: Discussionsupporting

confidence: 54%

Blunted DNA synthesis and delayed S-phase entry following inhibition of Cdk2 activity in the regenerating rat liver

Stärkel

Saeger

Sempoux

et al. 2005

Laboratory Investigation

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Activation of the cyclin E/Cdk2 complex may play an important role in mid-G1/S-phase progression in proliferating mammalian cells. We evaluated the effect of targeted inhibition of Cdk2 activity by CYC202 (Rroscovitine) on hepatocytes proliferation in vivo after 70% partial hepatectomy (PH) in rats. In controls, Cdk2 activity and DNA synthesis peaked 24 h after PH. CYC202 abrogated Cdk2 activity, prevented BrdU incorporation and PCNA expression and increased mortality 24 h after PH. Cyclin E and Cdk2 protein expression and complex formation was not affected by CYC202 nor was cyclin D1, Cdk4 and c-ras mRNA expression. Two consecutive injections 8 and 20 h after PH were required to elicit the inhibitory effect of CYC202, which was lost when either the injection at 8 h or at 20 h was withheld. Cdk2 activity and cell progression resumed 48 h after PH in surviving animals suggesting that CYC202 induced a reversible inhibition of the cell cycle. Our results confirm an important role for Cdk2 in hepatocytes proliferation in the regenerating liver. We demonstrate that molecular events, including Cdk2 activation, occurring within the 8th and 24th hour after PH (G1/S-phase transition) are crucial in determining whether or not DNA synthesis and hepatocytes proliferation proceed normally after PH.

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Section: Discussionsupporting

confidence: 54%

Blunted DNA synthesis and delayed S-phase entry following inhibition of Cdk2 activity in the regenerating rat liver

Stärkel

Saeger

Sempoux

et al. 2005

Laboratory Investigation

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“…Our studies of the same cells ( SW480, Calu-1, SK-N-SH, T24, peripheral blood lymphocytes) are broadly in agreement (DJW et al, unpublished data). Subsequent reports have used a restricted range of probes which would not distinguish the K-ras isoforms: HiHi 3 (Campisi et al, 1984;Ellis et al, 1981;Lockett and Sleigh, 1987;Sejersen et al, 1985), HiHi 380 (Ellis et al, 1981(Ellis et al, , 1982Goyette et al, 1984;Yaswen et al, 1985) and pY413 (George et al, 1985;Leon et al, 1987). Where PCR has been used, primers were chosen within exons 1 and 3 (Pal et al, 1993).…”

Section: Differential Expression Of K-ras Isoforms S Pells Et Almentioning

confidence: 99%

Developmentally-regulated expression of murine K-ras isoforms

et al. 1997

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“…Sci. USA, in press), c-ras (13,27,28), and c-fos (18,29,38) and genes encoding p53 (48, 60), actin (13,29,46) serum and that adenovirus infection preferentially activates genes whose expression reaches a maximum in the late G1-S phase. …”

mentioning

confidence: 99%

“…Sci. USA, in press), c-ras (13,27,28), and c-fos (18,29,38) and genes encoding p53 (48,60), actin (13,29,46), tubulin (46), and thymidine kinase (44). Other cell cycledependent genes have been identified as cDNA clones (17,31,43) by differential screening of cDNA libraries.…”

mentioning

confidence: 99%

Adenovirus type 2 activates cell cycle-dependent genes that are a subset of those activated by serum.

Liu¹,

Baserga²,

Mercer³

1985

Mol. Cell. Biol.

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We have studied a panel of 10 genes and cDNA sequences that are expressed in a cell cycle-dependent manner in different types of cells from different species and that are inducible by different mitogens. These include five sequences (c-myc, 4F1, 2F1, 2A9, and KC-1) that are preferentially expressed in the early part of the G, phase, three genes (ornithine decarboxylase, p53, and c-rasHa) preferentially expressed in middle or late G1, and two genes (thymidine kinase and histone H3) preferentially expressed in the S phase of the cell cycle. We have studied the expression of these genes in nonpermissive (tsAF8) and semipermissive (Swiss 3T3) cells infected with adenovirus type 2. Under the conditions of these experiments, adenovirus type 2 infection stimulates cellular DNA synthesis in both tsAF8 and 3T3 cells. However, four of the five early GI genes (c-myc, 4F1, KC-1, and 2A9) and one of the late G, genes (c-ras) are not induced by adenovirus infection, although they are strongly induced by serum. The other sequences (2F1, ornithine decarboxylase, p53, thymidine kinase, and histone H3) are activated by both adenovirus and serum. We conclude that the cell cycle-dependent genes activated by adenovirus 2 are a subset of the cell cycle-dependent genes activated by serum. The data suggest that the mechanisms by which serum and adenovirus induce cellular DNA synthesis are not identical.Cell cycle-dependent genes are operationally defined here as genes that are preferentially expressed in a specific phase of the cell cycle. A number of animal genes have already been identified whose expression is cell cycle dependent. These include histone genes (2, 22, 57), c-myc (13, 28, 35, 49; B. Calabretta, L. Kaczmarek, W. Mars, D. Ochoa, C. W. Gibson, R. R. Hirschhom, and R. Baserga, Proc. Natl. Acad. Sci. USA, in press), c-ras (13,27,28), and c-fos (18,29,38) and genes encoding p53 (48, 60), actin (13,29,46) serum and that adenovirus infection preferentially activates genes whose expression reaches a maximum in the late G1-S phase. MATERIALS AND METHODSCell line and culture conditions. tsAF8 cells are G1-specific, temperature-sensitive mutants originally isolated from BHK cells (12); these cells have been extensively characterized (3,12,25). Monolayer cultures are routinely maintained in Dulbecco modified Eagle medium containing 10% (vol/vol) donor calf serum at the PT of 34°C. To obtain quiescent (Go) cultures, tsAF8 cells are plated at 106 cells per 100-mm plate, grown to near confluence at 34°C, rinsed twice with prewarmed Hanks salt solution, fed with medium containing 0.5% (vol/vol) donor calf serum, and incubated for an additional 48 h at 34°C. Swiss 3T3 cells were cultured and made quiescent as previously described (47).Virus propagation, purification, and infection. Ad2 was grown in HeLa suspension cultures maintained in minimum essential modified suspension medium (Flow Laboratories, Rockville, Md.) with 5% fetal calf serum. Virus was purified as described previously (63)

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Regulated transcription of c-Ki-ras and c-myc during compensatory growth of rat liver.

Cited by 205 publications

References 40 publications

Blunted DNA synthesis and delayed S-phase entry following inhibition of Cdk2 activity in the regenerating rat liver

Blunted DNA synthesis and delayed S-phase entry following inhibition of Cdk2 activity in the regenerating rat liver

Developmentally-regulated expression of murine K-ras isoforms

Adenovirus type 2 activates cell cycle-dependent genes that are a subset of those activated by serum.

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